Cardiovascular Pathophysiology

Cardiovascular Pathophysiology

Learning Objectives

• Understand perfusion and cardiovascular pathophysiology, focusing on Hypertension and Hyperlipidemia.
• Understand Arrhythmias, focusing on Atrial Fibrillation (AF).
• Understand Stroke and Heart failure.
• Demonstrate nursing knowledge through inquiry.
• Integrate anatomy, physiology, and pathophysiology into clinical nursing practice.

Year 1 Recap

• Blood flow:
  • Right side to left side of the heart.
  • 3 types of circulation:
    • Systemic
    • Pulmonary
    • Coronary
• Areas that can go wrong:
  • Systemic blood flow
  • Coronary blood flow
  • Conduction system
• The cardiac cycle:
  • Atrial systole
  • Ventricular systole, phase 1
  • Ventricular systole, phase 2
  • Ventricular diastole, early
  • Ventricular diastole, late
• Heart conduction:
  • SA node → AV node → bundle of His → Purkinje fibers

ECG Overview

• Rate
• Rhythm
• Cardiac axis
• P waves
• PR interval
• QRS complex
• ST segment
• T waves

Perfusion

• Perfusion is the flow of blood through arteries and capillaries, delivering nutrients and oxygen to cells and removing cellular waste.
• Perfusion is the process of delivering blood to a capillary bed in its biological tissue to provide oxygen and nutrients to the cell
• Perfusion depends on blood volume, vascular resistance, and cardiac output.
• Ischemia = inadequate perfusion
• Infarction = cell death
• Cardiac output measures the amount of blood pumped out of the heart in one minute.
• Low blood volume is called hypovolemia.
• Cardiac output is made up of heart rate and stroke volume: $cardiac\ output = heart\ rate \times stroke\ volume$
• Heart Rate measures the speed at which the heart beats in one minute.
• Stroke volume (SV) is the quantity of blood pumped out of the left ventricle with every systolic contraction (heartbeat).
• Vascular resistance is the resistance present in the blood vessels.
• Perfusion of the heart muscle occurs during diastole via the coronary arteries.
• Perfusion of tissue in the body occurs during systole when the oxygenated blood is delivered to the tissue.
• Deoxygenated blood and waste are returned from the tissue to the circulation.
• These processes happen through hydrostatic and osmotic pressure.

Hypertension

• High blood pressure (hypertension) is when the force of your blood pushing against the walls of your blood vessels is consistently too high.
• Affects approx. 33.5% adult males and 28.3% adult females in NZ
• Only 16.7% of New Zealanders receive treatment for hypertension
• Hypertension is insidious, chronic, progressive, and a risk factor for cardiovascular and end-organ diseases, for example:
  • stroke
  • myocardial infarction
  • heart failure
  • atrial fibrillation
  • renal disease
  • cognitive decline

Hypertension Definitions

• Normotensive: $<120/80 mmHg$
• Intermediate: $120 -139/80-89 mmHg$
• Stage one (mild) hypertension: $>140/90 mmHg$ or average daytime ambulatory B/P of $>135/85 mmHg$
• Stage two (moderate) hypertension: $>160/100 mmHg$ or an average daytime ambulatory B/P of $>150/95 mmHg$
• Severe hypertension: systolic pressure of $>180 mmHg$ or a diastolic pressure of $>110 mmHg$
• Isolated systolic hypertension: systolic $>160 mmHg$ and diastolic $<90 mmHg$
• Isolated diastolic hypertension: diastolic $>90 mmHg$ and systolic pressure $<140 mmHg$
• For every 2 mmHg increase in systolic blood pressure the risk of death from ischaemic heart disease increases by 7%.
• For every 2 mmHg increase in systolic blood pressure the risk of stroke rises by 10%.

Assessment

• Urinalysis - hematuria and proteinuria
• Blood tests - creatinine and eGFR, electrolytes, HbA1c, lipid profile, BUN, FBC/CBC, LFTs
• Ophthalmoscopy examination of the fundus
• An ECG

Hypertension Risk Factors

Modifiable

• Obesity
• Sedentary lifestyle
• High fat, salt and/or sugar diet
• High alcohol intake
• Certain chemical substances
• Stress

Non-Modifiable

• Family history
• Gender
• Age
• Ethnicity
• Renal disease
• Diabetes

Diagnosing Hypertension

• Treatment is lifelong - essential that hypertension is accurately diagnosed
• Ambulatory monitoring is the gold standard for patients with a clinic blood pressure reading of $≥140/90 mmHg$
• If Ambulatory monitoring not available = three blood pressure readings over 3 –12 month period at different times of day as blood pressure varies throughout the day
• White-coat hypertension is defined as a difference of more than 20(systolic)/10(diastolic) mmHg between clinic and daytime out-of- clinic blood pressure measurements

Hypertension Treatment

• Management is patient dependent
• Give advice on diet, exercise, smoking, alcohol and caffeine consumption
• Antihypertensives – Angiotensin Converting Enzyme (ACE) inhibitors, Angiotensin Receptor Blockers (ARBs), Calcium Channel Blockers, beta blockers, thiazide diuretics

Blood Pressure Targets

• Are according to age and the presence of co-morbidities
• High risk: $>130/80mmHg$
• Intermediate risk: $>140/80mmHg$
• All people on drug treatment: $<130/80mmHg$
• Systolic > 120 mmHg is associated with a greater frequency of serious adverse effects in people with type 2 diabetes
• < 150/90 mmHg for very elderly = over 80 years

Complications of Hypertension

• Hypertensive heart disease
• Coronary artery disease
• TIA & angina
• Stroke (thrombotic and hemorrhagic stroke)
• Heart failure
• Aortic aneurysm
• Chronic kidney disease and kidney failure
• Research demonstrates that there is also a link between hypertension and dementia

Hyperlipidemia

• Hyperlipidemia is an elevation of one or more lipoproteins in the blood
• Cholesterol is transported to cells by lipoproteins that are either low density (LDL) or high density (HDL)
• LDL contributes to build up of fatty deposits as they transport cholesterol from the liver to the body's cells. This can eventually atherosclerosis
• HDL may actually reduce atherosclerotic build ups

Hyperlipidemia and Atherosclerosis

• Presence of LDL cholesterol attracts Macrophages and monocytes
• Foam cells are formed
• Recruitment of more inflammatory cells
• Plaque forms and eventually weakens endothelial wall and ulcerates
• Degradation of the fibrous cap
• Reduced release of nitrous oxide due to endothelial damage leading to vasoconstriction

Hyperlipidemia Risk Factors

• Sedentary lifestyle
• Poor diet
• Obesity
• Smoking
• Family history
• Age
• Diabetes

Hyperlipidemia Treatment

• Lowering of LDL-cholesterol is the primary indicator of optimum lipid management
• Statins
• Treatment should be based on an individual’s five-year CVD risk
• Statin treatment should be initiated for people with known CVD or at high CVD risk
• Starting doses:
  • For people with a five-year CVD risk of 5 – 15%, 10-20mg atorvastatin (titrate if needed to max of 80mg)
  • For people with known CVD or a CVD risk >15%, atorvastatin 10-40 mg (titrate if needed to max of 80mg)
• Diet and lifestyle advice is a big part of managing hyperlipidaemia

Hyperlipidemia Targets

• New Zealand guidelines group lipid profile targets:
  • total cholesterol less than $4 mmol/L$
  • LDL cholesterol less than $1.8 mmol/L$
  • HDL cholesterol greater than $1 mmol/L$
  • total cholesterol/HDL ratio less than 4
  • triglycerides less than $1.7 mmol/L$

Complications of Hyperlipidemia

• Atherosclerosis
• Angina
• Myocardial Infarction
• Stroke

Angina

• Angina is chest pain due to transient myocardial ischemia
• A result of Coronary Artery Disease (CAD)
• Angina symptoms occur when there is insufficient blood supply to the heart at times of increased oxygen demand
  • Physical activity
  • Emotional stress

Angina signs and symptoms

• Chest pain described as tight, dull, heavy or crushing
• Pain may radiate to the arms, neck, jaw or back
• Pain occurs during physical activity or emotional stress and relieved by rest
• Patient may have associated breathlessness, nausea, dizziness
• Angina pain is not usually sharp or stabbing or influenced by respiration

Diagnosing Angina

• Comprehensive history is critical
• Findings on physical examination and ECG are normal
• Blood tests: Lipid profile, TSH, LFTs, FBC, U&Es, BGL, trop T
• Referral for diagnostic assessment: stress testing/exercise ECG, echocardiogram, coronary angiography

Acute Coronary Syndromes (ACS)

Unstable Angina

• Reversible myocardial ischaemia
• Can be a warning of an impending infarction - approximately 20% will progress to acute MI
• Small fissure or superficial erosion of plaque that leads to transient episode of thrombotic vessel occlusion and vasoconstriction at site of plaque damage
• Thrombus is unstable and may occlude vessel for 20-30 minutes before return of perfusion
• Can present as new angina, angina at rest, or angina that is increasing in severity or frequency
• Dyspnea, diaphoresis, anxiety
• Form of acute coronary syndrome resulting from reversible ischemia

Treatment of Angina

• Different for stable angina and unstable angina
• Nitrates e.g Glyceril Trinitrate (GTN)
• Aspirin, statin, beta blockers, calcium channel blockers, possibly ACE inhibitor
• Patients need to have an angina action plan
• Use GTN before activities that are known triggers
• Stop what you are doing and rest
• Use GTN spray (one puff) or one tablet (or as directed)
• Take a second dose five minutes after the first dose if the pain has not eased
• Call an ambulance if the pain has still not eased five minutes after the second dose

Myocardial Infarction

• When an extended interruption of blood flow occurs (extended ischemia) this results in myocyte necrosis and results in myocardial infarction
• This is most commonly due to occlusion of a coronary artery following the rupture of a vulnerable atherosclerotic plaque
• ECG changes visible after 30-60 seconds of hypoxia
• Cardiac cells can sustain lack of oxygen for 20 minutes before cellular death occurs

Non-STEMI (Non ST-Elevation Myocardial Infarction)

• NSTEMI or Non-STEMI = Non ST Elevation Myocardial Infarction
• Account for 30% of Myocardial Infarctions
• Occurs by developing a complete occlusion of a minor coronary artery or a partial occlusion of a major coronary artery previously affected by atherosclerosis
• Causes a partial thickness damage of heart muscle

Diagnosing

• ECG with no ST segment elevation
• May have other ECG abnormalities
• Elevated Troponin T

STEMI (ST-Elevation Myocardial Infarction)

• Account for 70% of myocardial infarctions
• Occurs by developing a complete occlusion of a major coronary artery previously affected by atherosclerosis
• Causes a full thickness damage of heart muscle
• Urgent fibrinolysis treatment = reduction in mortality

Diagnosing

• Elevation of ST segment on ECG
• Elevated Troponin T

Assessment of Chest Pain

• History of presenting complaint
• Check for any associated symptoms
• Past medical history
• PQRST
• Vital signs
• ECG
• Cardiac enzymes
• Remember atypical symptoms

Treatment of Myocardial Infarctions

• GTN
• Aspirin
• IV morphine
• Oxygen if Spo2 <93%ra
• Fibrinolysis
• Percutaneous Coronary Intervention (PCI)
• Coronary Artery Bypass Graft (CABG)
• Long term medications

Acute Cardiovascular Diagnoses

• Pericarditis
• Endocarditis
• Myocarditis
• Cardiac tamponade

Disorders of the Aorta

• Aneurysms
  • Weakened areas of the vessel wall
  • If untreated an aneurysm may rupture
  • May be asymptomatic but may have dull pain as aneurysm gets bigger
• Dissection
  • Separation of the layers of the vessel wall
  • Sudden severe chest or upper back pain
  • Can be very quickly fatal

Cerebrovascular Accident (CVA) / Stroke

• Stroke is the third most common cause of death in New Zealand
• Incidence of stroke increases with age
• 25-30% of people who have a stroke will be under 65 years
• The number of people experiencing stroke will rise by 40% over the next decade.
• 75% of strokes are preventable

Stroke Diagnosis

• Symptoms sudden onset lasting more than 1 hour
• Loss of neurological function e.g. unilateral paralysis or numbness
• Maximal neurological deficit at the onset
• Focal due to loss of blood supply to one part of the brain

Ischemic Stroke

• An obstruction in a blood vessel supplying blood to the brain
• Accounts for approx. 85% of all stroke cases
• Atherosclerosis, thromboembolism, atrial fibrillation, vasculitis
• Can sometimes be seen on CT scan but MRI scan better for ischaemia

Ischemic Stroke Treatment

• “Time is brain”
• Thrombolysis – within 3 hours of symptom onset
  • Ateplase
• Endovascular thrombectomy
• Stroke units

Hemorrhagic Stroke

• An artery in the brain ruptures and leaks blood into the brain (intracranial haemorrhage).
• Causes swelling and pressure, which then leads to further damage and loss of function.
• Uncontrolled hypertension, aneurysm ruptures, arteriovenous malformations, head injury, arterial dissections
• Subarachnoid haemorrhage
• Intracerebral haemorrhage

Hemorrhagic Stroke Treatment

• Focus is controlling bleeding
• Emergency surgery may be required
  • Superficial temporal artery to middle cerebral artery bypass graft
  • Guglielmi coils
  • Aneurysm clipping

Trans Ischemic Attack (TIA)

• Temporary loss of neurological function due to reduced blood flow to brain but without tissue death
• Symptoms may be brief (minutes) but will last no longer than 24 hours
• Can be a warning of an impending stroke
• More than one in 12 people will have a stroke within a week after a TIA
• Symptoms same as stroke
• CT scan

TIA Treatment

• Aim of treatment is prevention of strokes
• Modifying stroke risk factors
• Medication Treatment may include antiplatelet drugs, anticoagulants and statins
• Carotid endarterectomy
• Arterial angioplasty (often with stenting)

Heart Failure

• Heart failure is a complex clinical syndrome resulting in significant impairment of quality of life and is associated with high morbidity and mortality
• Characterized by progressive cardiac remodeling with ventricular dilation and/or ventricular hypertrophy
• Impairment of ventricular filling or ejection of blood
• Reduced ability to cope with normal demands
• Can lead to Congestive Heart Failure (CHF) where fluid accumulates in tissues and organs

Heart Failure in NZ

• Heart failure affects approx. 2-3% of adults in New Zealand. There are approximately 12,000 hospital admissions related to heart failure each year
• Costs associated with heart failure are approx. 50 million per year
• Overall, heart failure affects at least 10 percent of people aged over 70 years. Within this group, about 50 percent die within 5 years of diagnosis.

Heart Failure Causes

• Coronary Artery Disease (CAD)
• Hypertension
• Recent Acute Coronary Syndrome (ACS)/Myocardial Infarction (MI)
• Myocarditis
• Cardiomyopathy
• Heart valve disease
• Atrial fibrillation (AF)
• Thyroid Disease
• Pregnancy
• Diabetes
• Age, gender, smoking, etoh use

Heart Failure Classifications

• Timeline of illness
• Ejection fraction
• Structure and progression of disease
• Symptom severity

Heart Failure Classifications

• New York Heart Association Functional Classification:
  • Class I: Patients with cardiac disease but without resulting limitation in physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, shortness of breath or anginal pain.
  • Class II: Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, shortness of breath or anginal pain.
  • Class III: Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary activity causes fatigue, palpitation, shortness of breath or anginal pain.
  • Class IV: Patients with cardiac disease resulting in an inability to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency or of anginal pain are present at rest. If any physical activity is undertaken discomfort is increased.

Left Sided Heart Failure

• Most common type of heart failure
• Heart failure with reduced ejection fraction(HFrEF), also called systolic failure
  • The left ventricle loses its ability to contract normally and pump with enough force to circulate blood.
  • Typically seen in structural heart disease, e.g IHD or cardiomyopathy
• Heart failure with preserved ejection fraction (HFpEF), also called diastolic failure
  • The left ventricle loses its ability to relax and fill due to stiffening of the muscle leading to reduced output.
  • Typically seen in the elderly or atrial fibrillation
• Blood builds up in pulmonary veins

Left Sided Heart Failure Signs and Symptoms

• Fatigue
• Weakness
• Orthopnea - sensation of breathlessness when lying down -relieved by sitting or standing
• Dyspnea (on exertion)-sensation of difficult breathing
• Pulmonary edema
• Tachycardia
• Tachypnea
• Shortness of breath
• Cough
• Pinkish/whitish frothy sputum
• Hypoxia
• Hypercapnia- Co2 retention -abnormally high concentration of CO2 in the blood

Right Sided Heart Failure

• Often occurs as a result of left sided heart failure
• Can be caused by primary respiratory disease = cor pulmonale
• Right side of heart cannot pump blood back to the lungs efficiently
• Back up of blood venous system = fluid shift into tissues and organs, leading to impaired function

Right Sided Heart Failure Signs and Symptoms

• Distended, pulsating neck vein (sit patient upright- more noticeable)
• Peripheral edema – weight gain, swollen ankles/feet
• Hepatomegaly and splenomegaly
• Ascites
• Anorexia and GI upset
• Dyspnea

Heart Failure Compensation

• There are three compensatory mechanisms to maintain blood flow to the tissues:

CNS

• Reduced cardiac output → increased sympathetic activity → increased heart rate and contractility

Increased pre-load

• The kidneys sense reduced renal blood flow → activate RAAS → sodium and water retention → increased blood volume(pre-load)

Cardiac hypertrophy

• Heart increases muscle mass → increased stroke volume

Heart Failure Decompensation

CNS

• Increased HR and contractility = increase the heart muscle’s demand for oxygen = eventually contributes to the heart failure

Increased pre-load

• Increased blood volume increases workload of heart = reduces ability of heart to pump increased volume effectively over time = eventually contributes to heart failure

Cardiac hypertrophy

• Heart increases muscle mass – hypertrophy –increases heart muscle’s demand for oxygen – eventually unable to maintain demand and contributes to heart failure
• Increased pressure inside the heart chambers over time (left ventricle most common)causes stretching of muscle fibres = reduces heart’s ability to pump effectively
• Cardiac Dilation

Imbalances in Heart Failure

• Acid base imbalances
• Electrolyte imbalances
• Fluid imbalances
• Due to:
  • Hearts failure to pump blood and perfuse tissue
  • Overstimulation of the RAAS
  • Treatment regimes

Investigations for Heart Failure

• ECG – LVH, LVF
• Chest X-ray – cardiomegaly, pulmonary edema
• Echocardiogram
• Blood Test - Brain Naturiectic Peptide (BNP)

Heart Failure Treatment

• Relieve & improve symptoms
• Decrease hospital admissions
• Improve quality of life
• Decrease mortality
• Diuretics is used first-line to reduce fluid overload
• ACE inhibitors or ARBs
• Beta blockers
• Spironolactone
• Digoxin
• Anticoagulants

Nursing Considerations for Heart Failure

• Get a good history from patient
• Careful discharge planning to avoid multiple readmissions
• Heart Failure Nurse referral
• Education:
  • Medication
  • Dietary
  • Exercise
  • Fluid management and balance (end stage – frequently have fluid restrictions)
  • Symptom monitoring - cough, dyspnea, peripheral edema, daily weight

Arrhythmias

• Normal heart rhythm = sinus rhythm
• An arrhythmia is defined as a heart rhythm that is irregular or abnormal
• An arrhythmia can be paroxysmal or continuous
• Cardiac arrhythmias Include:
  • Sinus arrhythmias
  • Atrial arrhythmias
  • Junctional arrhythmias
  • Ventricular arrhythmias (ventricular tachycardia or ventricular fibrillation)
  • Atrioventricular block

Common Arrhythmias

• Atrial fibrillation
• Supraventricular tachycardia (SVT)
• Sick sinus syndrome
• Atrial flutter
• Premature atrial contractions (PACs)
• Premature ventricular contractions (PVCs)
• Ventricular tachycardia
• Ventricular fibrillation
• Supraventricular arrhythmias
• Woolf-Parkinson-White syndrome

Supraventricular Tachycardia (SVT)

• Range of conditions where there is an abnormal impulse produced by or reliant on the AV node.
  • Atrioventricular nodal re-entrant tachycardia (AVNRT)
  • Atrioventricular reciprocating/re- entrant tachycardia (AVRT)
  • Atrial tachycardia (AT)
• More common in females than males
• Paroxysmal
• Various causes and triggers

SVT Symptoms

• Palpitations
• Pounding in the neck or head
• Chest discomfort (chest pain is unusual)
• Dyspnea
• Anxiety
• Light-headedness
• Fainting

SVT Diagnosis

• History of presenting complaint from patient
• ECG
• Blood tests

SVT Treatment

Short term

• Increasing vagal tone
  • Valsalva maneuver
  • Cold stimulus to face
  • Carotid sinus massage
• Chemical cardioversion
  • Adenosine
• Synchronized electrical cardioversion

Long term

• Pharmacological
  • Calcium channel blockers
  • Beta blockers
  • antiarrhythmics
• Surgical
  • Catheter/radiofrequency ablation

Atrial Fibrillation (AF)

• Atrial fibrillation (AF) is a cardiac arrhythmia characterized by rapid irregular contractions of the atria and irregular ventricular response
• Leads to reduced cardiac output
• Three types of AF:
  • Paroxysmal AF – Characterized by recurrent episodes of AF that last less than 48 hours or up to 7 days less and self terminate.
  • Persistent AF – Characterized by episodes of AF that last more than seven days. They do not self terminate but can be treated to return to a normal rhythm.
  • Permanent AF – AF that has been present for more than one year and has not responded to treatment.
• Prevalence increases with age

Atrial Fibrillation (AF)

• Electrical signals do not originate in the SA node
• Multiple impulses firing at once in atria
• Limited impulses travel through the AV node
• Incoordination between atria and ventricle

AF SIGNS AND SYMPTOMS

• Palpitations
• Shortness of breath
• Tachycardia
• Irregular pulse
• Tiredness, lethargy
• Dizziness, syncope
• Reduced exercise capacity
• Chest pains or chest tightness
• Hypotension

Complications of AF

• Thrombus formation
• Stroke
• Cardiomyopathy
• Heart Failure

AF Treatment

Treatment Aims:

• Symptom management
• Assessment and management of thromboembolic risk

Pharmacological Treatment:

• Beta blockers
• Calcium channel blockers (Verapamil or Diltiazem)
• Digoxin
• Amiodarone
• Anticoagulant therapy (warfarin, dabigatran, clopidogrel, rivaroxaban, aspirin)

Non Pharmacological Interventions:

• Cardioversion
• Catheter Ablation

Nursing Considerations

• Early recognition of AF
• Patient education
• Self-management plan
• Perioperative care